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Pathological sympathoexcitation: how is it achieved?
M Elam1, Y B Sverrisdottir, B Rundqvist
1Department of Clinical Neurophysiology, Inst for Clinical Neuroscience, Sahlgrenska University Hospital, Götenburg, Sweden.
Acta Physiologica Scandinavica
|March 1, 2003
Summary
Congestive heart failure and obstructive sleep apnoea syndrome increase sympathetic nerve activity through enhanced nerve firing and recruitment. These changes, particularly increased firing frequency, may pose a risk factor for neurotransmitter release.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Sleep Medicine
Background:
- Congestive heart failure (CHF) and obstructive sleep apnoea syndrome (OSAS) are linked to heightened sympathetic nervous system activity.
- Increased muscle sympathetic nerve activity (MSNA) is a common feature in both CHF and OSAS.
Purpose of the Study:
- To investigate the firing characteristics of single vasoconstrictor nerve fibres in patients with CHF and OSAS.
- To determine the mechanisms underlying augmented vasoconstrictor output in these conditions at rest and during sympathoexcitatory stimuli.
Main Methods:
- Microneurographic recordings of single vasoconstrictor fibres in the muscle vascular bed.
- Analysis of firing characteristics, including firing probability and within-burst firing, at rest and during simulated sympathoexcitatory stimuli.
Main Results:
- Both CHF and OSAS patients exhibit increased firing probability at rest.
- OSAS patients show increased multiple within-burst firing at rest, unlike CHF patients.
- Both groups demonstrate a shift towards multiple within-burst firing during sympathoexcitatory stimuli.
- Evidence suggests recruitment of previously inactive vasoconstrictor fibres contributes to transient responses.
Conclusions:
- Pathological sympathoexcitation in CHF and OSAS involves both increased firing frequency and fibre recruitment.
- A shift towards increased multiple within-burst firing may be an independent risk factor due to elevated neurotransmitter release.